Interdependence of a mechanosensitive anion channel and glutamate receptors in distal wound signaling
Jacob Moe‐Lange, Nicoline M. Gappel, Mackenzie Machado, Michael M. Wudick, Cosima S. A. Sies, Stephan Schott‐Verdugo, Michele Bonus, Swastik Mishra, Thomas Hartwig, Margaret Bezrutczyk, Debarati Basu, Edward E. Farmer, Holger Gohlke, Andrey V. Malkovskiy, Elizabeth S. Haswell, Martin J. Lercher, David W. Ehrhardt, Wolf B. Frommer, Thomas J. Kleist
Abstract
Glutamate has dual roles in metabolism and signaling; thus, signaling functions must be isolatable and distinct from metabolic fluctuations, as seen in low-glutamate domains at synapses. In plants, wounding triggers electrical and calcium (Ca 2+ ) signaling, which involve homologs of mammalian glutamate receptors. The hydraulic dispersal and squeeze-cell hypotheses implicate pressure as a key component of systemic signaling. Here, we identify the stretch-activated anion channel MSL10 as necessary for proper wound-induced electrical and Ca 2+ signaling. Wound gene induction, genetics, and Ca 2+ imaging indicate that MSL10 acts in the same pathway as the glutamate receptor–like proteins (GLRs). Analogous to mammalian NMDA glutamate receptors, GLRs may serve as coincidence detectors gated by the combined requirement for ligand binding and membrane depolarization, here mediated by stretch activation of MSL10. This study provides a molecular genetic basis for a role of mechanical signal perception and the transmission of long-distance electrical and Ca 2+ signals in plants.